Pharyngula » Lua Yarhttp://scienceblogs.com/pharyngula
Just another siteFri, 31 Jul 2015 11:01:18 +0000en-UShourly1http://wordpress.org/?v=4.2.3Olfactory nerves (student post)http://scienceblogs.com/pharyngula/2007/12/03/olfactory-nerves-student-post/
http://scienceblogs.com/pharyngula/2007/12/03/olfactory-nerves-student-post/#commentsMon, 03 Dec 2007 15:49:17 +0000http://scienceblogs.com/pharyngula/2007/12/03/olfactory-nerves-student-post/Today in class we learned about the functioning of olfactory nerves. It was really quite interesting, especially to find out how the olfactory system is organized. Let’s begin in the nasal cavity. Here, present in the mucus layer, are projections of the olfactory receptor cells. Each receptor cell is only capable of binding to one specific type of odorant molecule. These receptor cells travel through the porous bone separating the skull from the nasal cavity, and feed into a specific glomerulus. Glomeruli are located in the olfactory bulb, and have multiple receptors feeding into them. However, each glomerulus receives input from only one receptor type. In the glomerulus, the receptor neurons make excitatory connections with other cells, whose own axons project into the olfactory cortex in the brain. What is cool here is that there are about 1000 different types of olfactory receptor neurons, which each have their own proteins. This means that there are most likely 1000-2000 genes encoding for olfaction. It has been shown that this is not a combinatorial system like that developed for immunity.

Another cool thing I learned was that every time someone blows their nose, they are losing part of their brain. Seriously though, it’s not quite as bad as it sounds. What is really happening is that you are losing the olfactory receptor cells that protrude out into the mucus layer inside the nasal cavity. The neat thing is that these cells are able to regenerate, which is unusual for other human neural cells. I was wondering, if perhaps, due to the organization of the olfactory nerves, regeneration is able to happen because of the interaction between the olfactory receptor neurons and the glomeruli. Perhaps the protruding parts of the cells are able to be regenerated because they are actually only part of the cell, not the entire cell. If this is true, then if the glomerulus were destroyed, would that permanently destroy the sense of smell? Or would the glomerulus be capable of regeneration, like the olfactory receptor cells that feed into it?

]]>http://scienceblogs.com/pharyngula/2007/12/03/olfactory-nerves-student-post/feed/3Genetic link of OCD explored (student post)http://scienceblogs.com/pharyngula/2007/11/27/genetic-link-of-ocd-explored-s/
http://scienceblogs.com/pharyngula/2007/11/27/genetic-link-of-ocd-explored-s/#commentsTue, 27 Nov 2007 15:15:20 +0000http://scienceblogs.com/pharyngula/2007/11/27/genetic-link-of-ocd-explored-s/Researchers at Cambridge conducted a study that measured cognitive function and analyzed images of the brain in individuals with obsessive compulsive disorder (OCD). Magnetic resonance imaging (MRI) was used to capture images of each participants’ brain, and computerized tests were given to study the ability of the individual to stop repetitive behaviors. Also included in the study were healthy family members of the individuals with OCD, and healthy, unrelated individuals used as a control. The family members were included so that the genetic link behind OCD could be explored.

The researchers discovered that individuals with OCD and their relatives did worse on the computerized tasks than the healthy control group. When the MRI photos were analyzed, individuals with OCD and their relatives were found to have distinct patterns in their brain structure, namely a decrease in grey matter in brain regions associated with the suppression of responses and habits.

It was noted that this decrease in grey matter may contribute to the characteristic compulsive and repetitive behaviors associated with OCD. However, researchers are still a long way from discovering the genes involved with OCD, and further research needs to be done to explore why some family members with the altered brain structure do not develop OCD.

Since the family members have similar brain structure, there must be something else contributing to the development of OCD. I wonder if there is something going on inside that is causing a chemical imbalance that contributes to OCD, or if environmental factors are important in the development of OCD. It would be interesting to look at identical twins and see what the pattern of OCD is in them.

]]>http://scienceblogs.com/pharyngula/2007/11/27/genetic-link-of-ocd-explored-s/feed/13Prism-induced reversal of retinal images (student post)http://scienceblogs.com/pharyngula/2007/11/20/prisminduced-reversal-of-retin/
http://scienceblogs.com/pharyngula/2007/11/20/prisminduced-reversal-of-retin/#commentsTue, 20 Nov 2007 16:59:03 +0000http://scienceblogs.com/pharyngula/2007/11/20/prisminduced-reversal-of-retin/I was happily absorbed in my slightly vegetative stupor on the couch when my roommate walked into the room and starting talking about physics. Ugh, physics, I thought, but I politely listened as she began talking about lenses, specifically how they are related to sight. It is common knowledge that the images we see are inverted on the retina, and then further processed. However, my roommate was discussing experiments done on humans that inverted their vision by 180 degrees and found that, though at first they could not function normally, eventually they adapted. I thought this was fascinating, and wondered what the brain had to do with this process. Unfortunately my roommate’s knowledge was pretty limited, so I decided to do some research of my own.

Research on visual distortion of the retina has been going on for quite some time. Devices have been used that invert the retinal image, so that everything is seen upside down. At first subjects wearing this device will reach for things and miss, or will bump into things as they travel about a space. Eventually, they adapt. What I wanted to know is how do they adapt? What changes take place in the brain that allow them to do so? Is it just simply learning to reach a little farther to grab something, or walk a bit differently to avoid bumping into something? What is happening at the neural level?

What I discovered is that in order to make sense of the incorrect efferent sensory information, the subject must rely on perceptual and proprioceptive feedback (proprioceptive refers to the position sense, which is what allows us to perceive the location of various parts of the body). However, while the subject can adapt to this altered state of vision, it is not accompanied by a return to upright vision. Researchers found that the contralateral posterior parietal cortex is activated when subjects were trying to reach objects while their vision was distorted, and thus has an important role in visuospatial processing. Other studies indicated that there was no evidence of remapping of retinal coordinates. Further research needs to be conducted on neurons to see what (if anything) is occurring at the neural level. However, due to the rapid recovery of normal function after vision was restored, it seems unlikely that any major modifications were made. What I learned from this investigation is that changes seem to be taking place at the processing level that allow subjects to adapt. However, how this occurs still remains to be investigated.

]]>http://scienceblogs.com/pharyngula/2007/11/20/prisminduced-reversal-of-retin/feed/10Rapture of the Deephttp://scienceblogs.com/pharyngula/2007/11/12/rapture-of-the-deep/
http://scienceblogs.com/pharyngula/2007/11/12/rapture-of-the-deep/#commentsMon, 12 Nov 2007 09:49:37 +0000http://scienceblogs.com/pharyngula/2007/11/12/rapture-of-the-deep/In preparation for my trip to the Caribbean next semester, I spent this weekend taking a class to learn how to SCUBA dive. My class and I learned all about the necessary equipment, what to do in emergency situations, and how to stay safe while SCUBA diving. We also learned about the physics of pressure, volume and density, so that we could better understand what happens when you descend into the deep. This inevitably led to a conversation about Nitrogen narcosis.

Nitrogen narcosis, or “rapture of the deep”, is a condition in which the symptoms resemble those due to intoxication by alcohol. Divers experiencing nitrogen narcosis lose their decision making abilities, their focus, and their judgment, coordination and multitasking skills become impaired. What could this potentially mean for the diver? They could ignore safe diving practices because they feel invulnerable to the dangers of their surrounding environment (sounds a bit like the actions of those individuals who are intoxicated by alcohol).

While the mechanisms of narcosis are not fully understood, it is believed that the change in pressure due to depth has an impact on it (most cases are not reported until descent around 100 feet, and immediate relief from symptoms can be acquired simply by ascending a few feet). Nitrogen dissolves more slowly in the blood than other gases, which is thought to affect the permeability of the lipid bilayers of neural cells. The Meyer-Overton hypothesis states that narcosis is due to Nitrogen gas penetrating the lipids of the neural cells, which is thought to interfere with the transmission of neural cell signals. Further research has indicated that the gas induces an increase in volume of the bilayer, which disrupts the membrane environment and modifies cell responsiveness.

Luckily for me, I am only certified to dive to 60 feet, so I shouldn’t experience any complications due to Nitrogen narcosis. I’ll just play it safe and get drunk off alcohol instead.

]]>http://scienceblogs.com/pharyngula/2007/11/12/rapture-of-the-deep/feed/32Research into adult neural cell integrationhttp://scienceblogs.com/pharyngula/2007/10/30/research-into-adult-neural-cel/
http://scienceblogs.com/pharyngula/2007/10/30/research-into-adult-neural-cel/#commentsTue, 30 Oct 2007 19:42:13 +0000http://scienceblogs.com/pharyngula/2007/10/30/research-into-adult-neural-cel/I found an article about new brain cells that I thought was really interesting. Researchers at the Yale School of Medicine discovered the mechanism behind how new neural cells are integrated into the adult brain. It turns out that new neural cells take a while to mature and fully integrate themselves into existing neural networks in the brain. While they are maturing, they rely on signals from other brain regions so that they do not disturb ongoing functions of the brain. They can receive input from these other regions for up to 10 days before they are ready to make any of their own outputs. So how long does it take to fully develop their synaptic connections so that they can talk to one another? Up to 3 weeks.

So why do we care; what is significant about this discovery? This mechanism sheds light on how neural cells integrate themselves into existing networks, which will impact how stem cells are used to replace neurons lost to injury or disease. The main concern is about neurons firing inappropriately, which could cause seizures or cognitive dysfunction.

The full article can be found in the Journal of Neuroscience, Vol. 27

]]>http://scienceblogs.com/pharyngula/2007/10/30/research-into-adult-neural-cel/feed/2A fall break experience I do not care to repeathttp://scienceblogs.com/pharyngula/2007/10/25/a-fall-break-experience-i-do-n/
http://scienceblogs.com/pharyngula/2007/10/25/a-fall-break-experience-i-do-n/#commentsThu, 25 Oct 2007 21:16:37 +0000http://scienceblogs.com/pharyngula/2007/10/25/a-fall-break-experience-i-do-n/So while most of my fellow undergraduates were leaving town to go somewhere, anywhere, other than Morris for fall break, I had to stay behind. Sure, staying in Morris is not really all that bad, I mean, some people actually live here (sorry Professor). But I will be honest-it really is not on my list of top places to live. It is just, well, boring. I had to stay behind because I had some animals I had to take care of, and I will admit, I was looking forward to spending time lying in bed, working with my horses, and catching up on my senior seminar. Little did I know exactly how much time I would spend doing the first, and hardly any of doing the latter two.

Yep, this break I got floored with a virus. AND I literally mean floored. We shall call it the flu, because I had all the flu-like symptoms. Headache. Swollen lymph nodes. Achy neck and back. Fever. Achy stomach. Dizziness. So I spent a wonderful Saturday doing all the things a person my age would love to do, and then spent Sunday, Monday, Tuesday, Wednesday and some of today confined to my bed. Sure, you can say,

well you slept through most of it, so it couldn’t have been all that bad

But believe me, what little I was awake for was horrible. Mostly because it was absolutely gorgeous outside, I didn’t have any classes to attend, and yet my body was waging a war inside of me.

So, I understand the basic principle of how viruses work, but how can one virus have a multitude of diverse symptoms? What’s with the headache, and the achy joints? Do viruses affect neurons the same way they can affect other cells? Do they even invade neural cells?

]]>http://scienceblogs.com/pharyngula/2007/10/25/a-fall-break-experience-i-do-n/feed/1Mutations in the CFTR gene cause Cystic Fibrosishttp://scienceblogs.com/pharyngula/2007/10/19/mutations-in-the-cftr-gene-cau/
http://scienceblogs.com/pharyngula/2007/10/19/mutations-in-the-cftr-gene-cau/#commentsFri, 19 Oct 2007 18:10:13 +0000http://scienceblogs.com/pharyngula/2007/10/19/mutations-in-the-cftr-gene-cau/So one of the questions on our Neurobiology test due today was to see if there were any heritable diseases in humans that are caused by defects in ion channel genes. I discovered that mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene have been linked to Cystic Fibrosis (CF).

CF is a genetic disease that affects the lungs and digestive system of its victims. The defective CFTR gene produces a thick, sticky mucus that provides an environment for life-threatening pathogens to establish an infection, and can clog the lungs. This unusually thick mucus also interferes with the pancreas, and impairs the enzymes that help to break down food and allow the body to absorb it. The symptoms of CF include frequent lung infections; persistent coughing, oftentimes accompanied by phlegm; wheezing or shortness of breath; poor growth or weight gain, despite a healthy diet and appetite; salty tasting skin; and difficulty in bowel movements or greasy, bulky stools. The incidence is about one thousand new cases a year.

This mutation affects the physiology of the affected cells in many different ways. CF patients with pancreatic problems show a reduced ability to transport bicarbonate, which coincides with the evidence that CFTR regulates a chloride-coupled bicarbonate transport. The importance of bicarbonate is that it affects the pH of the cells. Thus, because CF patients have defective CFTR proteins, they secret a more acidic fluid, whereas normal tissues secrete an alkaline fluid. Bicarbonate and pH levels are important because they affect bacterial binding to cells, with the CF condition (more acidic) being more conducive to bacterial binding. This was demonstrated in a study by Choi et al. (2001), from which they concluded that bicarbonate transport was important in the functioning of secretory epithelial cells, and thus has implications for CF.

One interesting proposal is that mutations in the CFTR gene are still prevalent in the human population because the heterozygous condition may convey increased resistance to infectious diseases. In a study by Pier et al. (1998), it was discovered that the bacterium that causes typhoid fever, Salmonella typhi, uses the CFTR protein to enter into epithelial cells. So in CF patients, with defective CFTR proteins, S. typhi is not as able to attach to and invade epithelial cells, and thus less likely to establish an infection.

]]>http://scienceblogs.com/pharyngula/2007/10/19/mutations-in-the-cftr-gene-cau/feed/0Lua’s thoughts on the Soul Made Flesh readinghttp://scienceblogs.com/pharyngula/2007/10/12/luas-thoughts-on-the-soul-made/
http://scienceblogs.com/pharyngula/2007/10/12/luas-thoughts-on-the-soul-made/#commentsFri, 12 Oct 2007 18:02:40 +0000http://scienceblogs.com/pharyngula/2007/10/12/luas-thoughts-on-the-soul-made/While I was reading the assigned chapters of the book Soul Made Flesh (Zimmer, 2004) for class this past week, I came upon the story of the physician Thomas Sydenham. He was particularly good at making careful bedside observations while he was treating patients. In fact, he made the observation that diseases acted the same in everyone, and they were not unique to an individual. He made careful notes on disease symptoms, and even suggested that perhaps diseases should be treated as if they are individual species.

Sydenham’s work turned out to be controversial, because when prescribing a treatment, sometimes he would not use the traditional one, but instead would experiment with different treatments. Other physicians wanted to get his license revoked because his experimentation outraged them, even though Sydenham documented which treatments seemed to work better. We discussed this a bit in class, but I want to know why his new treatments were so controversial. If he devised his treatments in a manner that seemed logical, and he had experimental evidence to back it up, why was there such resistance? Is it perhaps that people could not accept that traditional treatments really did not work, and that they may now be responsible for the deaths of many people that could have been saved? Or is it simply a matter of people not being able to accept that things change?

The creation of new neurons, known as neurogenesis, is an important process. It is by this process that the brain forms, and most of it occurs during pre-natal development. An early theory proposed by neuroanatomists that has recently been refuted by experimental evidence is that adult neurogenesis does not occur. In adult neurogenesis, it has been observed that most of the new neurons die shortly after their formation, while only a few become integrated into the functioning structure of the brain. So what is the significance of adult neurogenesis?

While the functioning of this process is not known, it has been speculated that it is important for memory and learning processes, and is linked to stress. Stress causes a lot of people a lot of harm, and has been linked to many disorders, such as depression. Depression is a condition that is regulated by antidepressants. Know what other activity is regulated by the activity of antidepressants? You guessed it, NEUROGENESIS! A recent study showed that the brain responds to stress-relieving situations, such as those that build learning and memory, with increased neurogenesis. Stressful situations, such as those that induce physiological or psychological stress, are marked by decreased neurogenesis. A decrease in neurogenesis has been indicated to be a key factor in the progression of depression.

Of course, there are individuals out there who have reported experiments that refute the process of adult neurogenesis. One author speculates on whether or not there is true scientific evidence to back these findings, and that perhaps the new cells being formed are glial cells.

So, how can one keep the level of neurogenesis up and reduce depression? By removing oneself from physiologically and psychologically stressful situations, and getting some exercise.

Where do people get the idea that intelligence has a biological basis? Oh yeah, from those geneticists, whose research has shown that intelligence levels can be inherited. One fairly new development for researching intelligence is through the conduction of brain imaging studies.

Recently, two neuroscientists by the names of Richard Haier of the University of California, Irvine and Rex Jung of the University of New Mexico, compiled a review of 37 such intelligence imaging studies. With this data, and current neurobiology studies that indicate intelligence is a measure of how well information travels through the brain, Haier and Jung formulated what they call the Parieto-Frontal Integration Theory (P-FIT). This theory identifies the stations of the brain, chiefly found in the frontal and parietal lobes, that network to produce intelligent information processing. So, whether you are smart or stupid depends, in part, on differences in connections between, and composition of, specific areas of the brain.

Haier and Jung have made many contributions to intelligence research. They discovered that it is unlikely that a single “intelligence center” exists, as the regions of the brain related to general intelligence are dispersed throughout the brain. In another study, general intelligence levels between the sexes were determined to have essentially no disparity, and yet their neural structures are different, with women having more white matter and men having more gray. This indicates that intelligence levels are independent of brain design.

Of course, can all of this just be taken with a grain of salt, because how does one really measure intelligence?